Diabetes, DKA, HHS, Hypoglycemia Flashcards

1
Q

When insulin goes up _____ goes down, when _____ goes down, insulin goes up

A

Cortisol
Growth hormone
Epinephrine
Glucagon

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2
Q

Why is insulin so important?

A

Insulin is the key that lets glucose into the cells

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3
Q

How long should be patient be fasting before taking a fasting glucose?

A

8 hours

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4
Q

Fasting glucose more than ___ indicates diabetes

A

126 mg/dL

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5
Q

What is an A1C

A

3 month average of the patients blood glucose, glucose sticks to the hemoglobin and the more glucose that stuck, the higher

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6
Q

Normla A1C is

A

5.6%

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7
Q

A1C range for pre diabetes is

A

5.7% - 6.4%

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8
Q

A1C high than ___ indicates diabetes

A

6.5%

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9
Q

Higher than ___ during a 2 hour glucose tolerance test indicates diabetes

A

200 mg/dL

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10
Q

What random plasma glucose level plus s/s what hyper/hypoglycemic indicates diabetes?

A

more than 200 mg/dL

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11
Q

Type 1 diabetes pathology

A
  1. Autoimmune + environmental trigger
  2. T cell mediated destruction of pancreatic beta cells
  3. Reduces beta cell functioning by 80-90% before hyperglycemia and other s/s occur
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12
Q

What age does type 1 diabetes occur at?

A

any age

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13
Q

Are men or women more genetically predisposed?

A

Men are
Women - 2.1%
Men - 6.1%

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14
Q

Type 2 diabetes pathology

A
  1. insulin resistance

2. Beta cell destruction

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15
Q

If one parent, both parents or a first degree relative has diabetes what is the chance that the child will have diabetes?

A

1 parent: 40% lifetime risk
Both parents: 70% lifetime risk
First-degree relative: 3X likely

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16
Q

TCF7L affects

A

insulin secretion and glucose production

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17
Q

ABCC8 helps

A

regulate insulin

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18
Q

CAPN1O is associated with

A

type 2 diabetes

Risk in Mexican Americans

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19
Q

GLUT2 helps

A

move glucose into the pancreas

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20
Q

GCGR is

A

glucagon hormone involved in glucose regulation

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21
Q

Type 2 diabetes affects GI by…

A

decreases incretin effect

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22
Q

Type 2 diabetes affects fat by…

A

increased lipolysis

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23
Q

Type 2 diabetes affects kidney by…

A

increasing glucose reabsorption

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24
Q

Type 2 diabetes affects muscles by…

A

decreased glucose uptake

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25
Q

Type 2 diabetes affects the brain by…

A

neurotransmitter dysfunction

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26
Q

Type 2 diabetes affects liver by…

A

increased hepatic glucose production

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27
Q

Type 2 diabetes affects pancreas by…

A

increased glucagon secretion and impaired insulin secretion

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28
Q

Other causes of diabetes include? (7)

A
  1. Pancreatic disorders
  2. Hormonal disorders (Cushing, acromegaly)
  3. Cystic fibrosis
  4. Down syndrome
  5. Hemochromatosis
  6. Drug induced
  7. Trauma/infection
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29
Q

What medications can cause drug induced diabetes? (5)

A
  1. Nicotinic acid
  2. Glucocorticoids
  3. Anti-rejection meds
  4. HIV/AIDS meds
  5. Chemotherapy
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30
Q

What is hemochromatosis?

A

autosomal recessive disorder characterized by an increase in iron absorption by GI and increased total body iron stores. Excess iron sequestered in different tissues including liver, endocrine and exocrine pancreas and the pituitary

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31
Q

Metformin is…

A

First line therapy

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32
Q

Metformin

A

MOA: Decreases insulin resistance and hepatic glucose production (stops making excess glucose
Dosing: 500mg titrated 2000-2500mg
SE: GI, Vitamin B deficiency
Contraindicated: pt. with GFR <30

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33
Q

What does a vitamin B12 deficiency look like?

A

Neuro s/s

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34
Q

What are patients on metformin at risk of developing?

A

Lactic acidosis

Major risk when patients are given contrast so usually stopped while in the hospital

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35
Q

How do you treat diabetes if the patient has a history of heart disease or stoke (ASCVD)?

A

start with a GLP-1

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36
Q

GLP-1 receptor agonist

A

MOA:
Dosing: slow and gradually increase
SE: GI - N/V
Contraindicated: some have renal adjustments

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37
Q

What GLP-1 receptors agonist are helpful with the heart and kidneys?

A

Dulaglutide
Liraglutide
Semaglutide

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38
Q

SGLT2 inhibitors (flozin)

A

MOA: pee out sugar
SE: GU infections, dehydration, hypotension, euglycemic DKA, NPO, bone fracture
Contraindications: renal dosing considerations

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39
Q

DPP4I

A
MOA: slows the inactivation of incretin hormones by DPP-4 enzyme
SE: severe joint pain, rash/blisters 
Contraindications: NYHA class III or IV
** doesn't do much to decrease blood glucose, only really decrease use of insulin and decrease rate of hypoglycemia
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40
Q

Sulfonylureas

A

MOA: stimulates beta cells
Dose: low and titrate as needed
SE: hypoglycemia
CAUTION: renal and liver patients

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41
Q

Thiazolidinedione

A

MOA: stimulates insulin uptake in muscles cells and makes you more sensitive to insulin at peripheral and liver
SE: edema, weight increase (d/t peripheral edema)
Can also be used in pt. with fatty liver disease or NASH

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42
Q

Basal insulin is

A

Immediate or long acting insulin

Covers the body regular glucose production (normal hepatic and renal glucose output)

43
Q

Bolus insulin

A

Short or rapid acting insulin

Manages mealtime glucose

44
Q

Basal: NPH

A

Onset: 2-4 hours
Peak: 8-12 hours
Duration: 12-20 hours

45
Q

Basal: Glargine (lantus)

A

Onset: 1-2 hours
Peak: minimal
Duration: 20-24 hours

46
Q

Basal: Glargine (Toujeo)

A

Onset: 1-2 hours
Peak: none
Duration: 24-26 hours

47
Q

Basal: Detemir (levemir)

A

Onset: 1-2 hours
Peak: minimal
Duration: 18-24 hours

48
Q

Basal: Degludec (tresiba)

A

Onset: 1-2 hours
Peak: none
Duration: 36 hours

49
Q

Bolus: Fast acting aspart or fast acting lispro

A

Onset: 2-15 mins
Peak: 1-2 hours
Duration: 3-5 hours

50
Q

Bolus: Lispro

A

Onset: Less than 15 minutes
Peak: 1-2 hours
Duration: 3-5 hours

51
Q

Bolus: Aspart

A

Onset: Less than 15 minutes
Peak: 1-2 hours
Duration: 3-5 hours

52
Q

Bolus: Gluliaine (apidra)

A

Onset: Less than 15 minutes
Peak: 1-2 hours
Duration: 3-5 hours

53
Q

Bolus: Regular

A

Onset: 30-60 minutes
Peak: 3-4 hours
Duration: 6-8 hours

54
Q

Premixed insulins: novolin 70/30 and humulin 70/30

A

Onset: 30-60 minutes
Peak: 2-10 hours
Duration: 10-18 hours

55
Q

Premixed insulins: humalog 75/25 and Novalog 70/30

A

Onset: 10-30 minutes
Peak: 1-6 hours
Duration: 10-24 hours

56
Q

What are the two insulins that can be bought over the counter?

A

NPH and regular

57
Q

What are the nursing considerations for giving insulin?

A
  1. Training patients on proper injections
  2. Timing of injection
  3. Rotation of sites
  4. Cloudy insulins need to be mixed
58
Q

What is the most common precipitating factor of DKA and HHS?

A

infection including DM ulcer and sepsis

59
Q

What are other precipitating factors/stressors for DKA? (7)

A
  1. Non-compliance with medical treatment or monitoring
  2. Alcohol/cocaine
  3. Cardiovascular event
  4. Trauma
  5. Corticosteroids
  6. Antipsychotic meds
  7. Acute GI disease (pancreatitis)
60
Q

What are other precipitating factors/stressors for HHS? (9)

A
  1. Non-compliance with medical treatment or monitoring
  2. Alcohol/cocaine
  3. Cardiovascular event
  4. Trauma
  5. Corticosteroids
  6. Antipsychotic meds
  7. Acute GI disease (pancreatitis)
  8. CHF
  9. Renal dysfunciton
61
Q

What are the typical lab values for DKA?

A
Glucose: >250
pH: <7.3
Bicarb: <15
Serum osmolarity: <320
Anion gap: >12
Urine and serum ketones: moderate-high
62
Q

What are the typical lab values for HHS?

A
Glucose: >600
pH: >7.3
Bicarb: >15
Serum osmolarity: >320
Anion gap: variable
Urine and serum ketones: none/trace
63
Q

Mild DKA lab values:

A
Glucose: >250
pH: 7.25-7.35
Bicarb: 15-18
Anion gap: >10
Urine and serum ketones: positive
Mental status: alert
64
Q

Moderate DKA lab values:

A
Glucose: >250
pH: 7.00-7.24
Bicarb: 10-15
Anion gap: >12
Urine and serum ketones: positive
Mental status: alert/drowsy
65
Q

Severe DKA lab values

A
Glucose: >250
pH: <7.00
Bicarb: <10
Anion gap: >12
Urine and serum ketones: positive
Mental status: stupor/coma
66
Q

What are two things that lead to DKA?

A
  1. Absolute insulin deficiency

2. Stress, infection, or insufficient insulin intake

67
Q

When this DKA happens which hormones change and do they increase or decrease?

A
  1. Glucagon
  2. Catecholamines
  3. Cortisol
  4. GH
    ALL INCREASE
68
Q

What processes increase during DKA?

A

lipolysis, proteolysis, and glycogenolysis

69
Q

What processes decrease during DKA?

A

protein synthesis and glucose utilization

70
Q

What will eventually happen to the body due to DKA? (9)

A
  1. Increase gluconeogenic substrates
  2. Increase gluconeogenesis
  3. Hyperglycemia
  4. Glucosuria (osmotic diuresis)
  5. Loss of water and electrolytes
  6. Dehydration
  7. impaired renal function
  8. Hyperosmolarity
  9. lactic acidosis
71
Q

What will the CO2 and lactate level be with DKA?

A

CO2: 21-31
Lactate: high

72
Q

What are the s/s of DKA? (11)

A
  1. Tachycardia and hypotension
2. Orthostatic BP and pulse changes 
3. Increased urination
  2. SOB
5. AMS
6. Thirst (polydipsia)
7. Dehydration 
8. Poor skin turgor 
9. N/V
  3. Abdominal pain
  4. Kusmauls respirations
73
Q

What are the s/s of HHS? (9)

A
  1. Tachycardia and hypotension
  2. Orthostatic BP and pulse changes
  3. Increased urination
  4. Hyperosmolarity (>320)
  5. AMS
  6. Thirst (polydipsia)
  7. Dehydration
  8. Poor skin turgor
  9. N/V
74
Q

What lab tests should be ordered STAT for DKA?

A
  1. BMP
  2. Mg
  3. CBC
  4. UA
  5. Serum ketones
  6. ABG
75
Q

Additional tests orders for DKA might be?

A
  1. CXR
  2. EKG
  3. Lipase
  4. Hepatic function panel
  5. Lactate
  6. Trop
  7. Blood cultures X2
  8. Urine culture
76
Q

What monitoring should you do for a patient with DKA?

A
  1. VS every hour
  2. I&O
  3. Cardiac or telemetry monitoring
77
Q

What fluids should be used in DKA?

A
  1. Bolus fluids: 2-4 liters of NS infused over 1 hour

2. Maintenance fluids: NS or 0.45 NS for 150-250 ml/hr

78
Q

When should you switch to D5 0.45% NS in DKA? What rate?

A

when the blood glucose is 250 or less

Rate: 150-250 ml/hr

79
Q

When should you switch to D5 0.45% NS in HHS? What rate?

A

when the blood glucose is 300 or less

Rate: 150-250 ml/hr

80
Q

What medications should be given in the treatment of DKA?

A
  1. Insulin: bolus 10 units of regular insulin and start IV infusion
  2. Treat underlying patho like infection with antibiotics
81
Q

What is the role of potassium in DKA/HHS?

A

Potassium determines when you can start the insulin drip. Potassium needs to be a normal range before starting.

82
Q

K+<3.3

A

Hold insulin
Give 20-30mEq K+
Add insulin when potassium reaches 3.3

83
Q

K+: 3.3-5.1

A

Give 20-30mEq K+ to keep potassium between 4-5

Continue insulin

84
Q

K+ >5.2

A

Do not give K+
q2 serum K+ checks until below 5.2
Then add K+
Continue insulin

85
Q

How do you know when DKA has been resolved?

A
  1. Mental status recovered
  2. Blood glucose: 250 or less
  3. AG: less than 12 (closed anion gap)
  4. Bicarb: 18 or more
  5. Venous pH: more than 7.3
86
Q

Fluids for HSS are?

A

same as DKA

  1. Bolus fluids: 2-4 liters of NS infused over 1 hour
  2. Maintenance fluids: NS or 0.45 NS for 150-250 ml/hr
87
Q

Medications for HHS are?

A
  1. Insulin bolus: 10 units regular insulin IV
  2. Insulin infusion
  3. Treat underlying patho
  4. SubQ insulin if needed
88
Q

What are the risk factors of HHS? (4)

A
  1. Serious concurrent illness like MI or stroke
  2. Sepsis
  3. Pneumonia
  4. Debilitating condition (prior stroke or dementia)
89
Q

Pathology of HHS

A
  1. Hyperglycemia with blood glucose above 600
  2. Hyperosmolarity
  3. Non-ketotic because body is still producing insulin
90
Q

When is HHS resolved?

A

when the patients mental status has returned. Continue IV fluids and insulin until then

91
Q

What is the blood glucose for level 1 hypoglycemia?

A

54-70

92
Q

What is the blood glucose for level 2 hypoglycemia?

A

less than 54

93
Q

What is level 3 hypoglycemia characterized by?

A

A severe event characterized by altered mental and/or physical status requiring assistance

94
Q

In hospitals hypoglycemia..

A

causes a prolonged length of stay

Considered a never event

95
Q

When blood sugar gets low, what is released?

A

Glucagon and epinephrine is released

96
Q

What happens when glucagon is released in response to hypoglycemia?

A

glyconeogenesis –> gluconeogenesis –> increase hepatic glucose release

97
Q

What happens when epinephrine is released in response to hypoglycemia?

A

Reducing glucose up-take
Enhances production of hepatic glucose
Occurs around a blood sugar of 68
** reason for a lot of s/s of hypoglycemia

98
Q

What are the neurologic symptoms of hypoglycemia? (5)

A
  1. Diaphoresis
  2. Palpitations
  3. Apprehension/anxiety
  4. Tremor
  5. HTN
99
Q

What are the neuroglycopenic symptoms of hypoglycemia? (9)

A
  1. Cognitive impairment
  2. Fatigue
  3. Dizziness
  4. Visual changes
  5. Seizures
  6. Hunger
  7. Inappropriate behavior
  8. Abnormal behavior
  9. Convulsions
100
Q

What are the risk factors for hypoglycemia? (5)

A
  1. Hypoglycemia unawareness - occurs often so body thinks its normal and no s/s
  2. Advanced age - decreased ability to sense it
  3. Renal failure
  4. Liver disease
  5. AMS - can’t tell hypoglcemic
101
Q

Triggering event of hypoglycemia are? (8)

A
  1. Emesis
  2. decreased oral intake
  3. New NPO status
  4. Sudden reduction of steroid dose
  5. Medication errors
  6. Severe illness
  7. Alcohol/drugs
  8. Exercise
102
Q

How do you treat hypoglycemia if patient is alert and able to drink?

A

give 15-20 grams of a rapid acting carb like juice

103
Q

How do you treat hypoglycemia if patient is alert and awake but NPO or unable to swallow

A

give 25mL of 50% dextrose via IV and start dextrose 5% in water at 100ml/hr

104
Q

How do you treat hypoglycemia if patient with altered LOC?

A
  1. IV access: give 25mL of 50% dextrose via IV and start dextrose 5% in water at 100ml/hr
  2. No IV access: give glucagon 1mg IM, limit 2 times